ArticleOpen medicine (Warsaw, Poland)2022
lncRNA HAGLR modulates myocardial ischemia-reperfusion injury in mice through regulating miR-133a-3p/MAPK1 axis.
Article in Open medicine (Warsaw, Poland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Machine learning-based prediction of drug response in ischemia reperfusion animal model.Scientific reports · 2025Article
- Spotlight on HOX cluster‑embedded antisense lncRNAs in cardiovascular diseases (Review).International journal of molecular medicine · 2023Review
- LncRNA HAGLR silencing inhibits IL-1β-induced chondrocytes inflammatory injury via miR-130a-3p/JAK1 axis.Journal of orthopaedic surgery and research · 2023Article
- A novel long noncoding RNA AC125257.1 facilitates colorectal cancer progression by targeting miR-133a-3p/CASC5 axis.Open medicine (Warsaw, Poland) · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myocardial infarction is one of the leading causes of morbidity worldwide, but the underlying mechanism responsible for myocardial ischemia-reperfusion (I/R) injury remains elusive. lncRNA plays roles in inflammatory response, cell apoptosis and regulation of myocardial ischemia. However, whether lncRNA HAGLR could regulate myocardial I/R injury and the molecular mechanism need to be further investigated. lncRNA has been shown to bind to miRNAs and compete with endogenous RNAs. miR-133a-3p has been shown to regulate cardiomyocyte apoptosis and ischemic myocardial injury. In this work, it has shown that knockdown of HAGLR could suppress inflammatory response and cell apoptosis induced by I/R and, thus, alleviate myocardial I/R injury. HAGLR promoted myocardial I/R injury by inhibiting miR-133a-3p to promote MAPK1 expression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.